Lung–kidney system ↗Kidney integrates three input classes
Afferent-arteriolar stretch, macula-densa sodium chloride delivery, and renal sympathetic signaling influence renin release.
KIDNEYS + HEART / 07
Defend perfusion.
Then close the loop.
The renin–angiotensin–aldosterone system responds to renal perfusion, distal sodium delivery, and sympathetic context. It changes vascular, tubular, hormonal, and behavioral outputs.
Renin cleaves angiotensinogen
Renin initiates peptide processing that produces angiotensin I and, through ACE and other routes, angiotensin II.
Angiotensin II changes vascular tone
AT1-receptor signaling can increase systemic resistance and alter renal arteriolar tone, supporting pressure and filtration in acute volume loss.
Proximal sodium transport increases
Angiotensin signaling can favor proximal sodium and bicarbonate reabsorption and recruit thirst and ADH-related behavior.
Aldosterone changes distal transport
Mineralocorticoid signaling increases epithelial sodium-channel and pump activity while influencing potassium and hydrogen secretion.
Sodium and water influence volume
Renal retention changes extracellular volume, venous return, cardiac output, congestion, and pressure according to heart and vessel context.
Improved perfusion restrains renin
Restored pressure and distal delivery, natriuretic peptides, and other feedback signals can reduce continued RAAS activation.
RAAS blockade changes several stages
ACE inhibitors and ARBs alter angiotensin, aldosterone, efferent tone, sodium, potassium, and filtration context and therefore require monitoring.